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Chapters (40)
  1. Cover Page
  2. Title Page
  3. Dedication
  4. Prologue A Brief History of Banting
  5. Part One
  6. Chapter 1
  7. Chapter 2
  8. Chapter 3
  9. Chapter 4
  10. Part Two
  11. Chapter 5
  12. Chapter 6
  13. Chapter 7
  14. Chapter 8
  15. Chapter 9
  16. Chapter 10
  17. Chapter 11
  18. Chapter 12
  19. Chapter 13
  20. Part Three
  21. Chapter 14
  22. Chapter 15
  23. Chapter 16
  24. Chapter 17
  25. Chapter 18
  26. Chapter 19
  27. Chapter 20
  28. Chapter 21
  29. Chapter 22
  30. Chapter 23
  31. Chapter 24
  32. Epilogue
  33. Notes
  34. Bibliography
  35. Acknowledgments
  36. Illustration Credits
  37. A Note About the Author
  38. Also by Gary Taubes
  39. Footnotes
  40. Copyright

One is Jean Mayer’s glucostat hypothesis or, technically, the glucostatic regulation of food intake, and it is invoked to explain the short-term initiation of meals. Receptors in the hypothalamus, said Mayer, metabolize glucose, initiating the sensation of hunger when the available supply of glucose falls, and provoking satiety when it rises. This glucostatic regulation, as Mayer put it, is an “essential component of the mechanism by which the needs of the body make themselves felt in the satiety centers.” It couldn’t be the only one, however, because it offered no explanation for what Mayer called “the problem of the nature of the very fine adjustment knob…the mechanism which will make you regain the weight you lost after an illness, and which makes so difficult the maintenance of weight loss after an arduous weight reduction course.”

The second hypothesis, what the Cambridge University physiologist Gordon Kennedy called lipostatic regulation or the lipostat, would evolve in the 1970s into the remarkably durable notion that we are all endowed with a certain set point of body weight or adiposity that we defend against both caloric deprivation and (perhaps less vigorously) caloric surplus. By Kennedy’s logic, the lipostat is also located in the hypothalamus and accomplishes its fine-tuning job by monitoring the amount of fat in the body or some by-product of metabolism that is released into the bloodstream in relationship to our adiposity. When this adiposity signal dips below an acceptable level—the set point—the lipostat responds by increasing food intake or decreasing energy expenditure. When the adiposity signal moves above this set point, the lipostat works to suppress food intake and perhaps increase expenditure. According to this hypothesis, the fundamental difference between the lean and the obese is the amount of fat stores that the hypothalamus is set to defend—the set point—not the manner or vigor with which it is defended. Whatever our weight, if we find ourselves in a situation where our current level of body fat is beneath that of our set point, we will fatten easily until we’ve reached our predetermined level.